OTULIN deficiency causes auto-inflammatory syndrome

Research output: Contribution to journal › Journal article › Commissioned

Standard

OTULIN deficiency causes auto-inflammatory syndrome. / Fiil, Berthe Katrine; Gyrd-Hansen, Mads.

In: Cell Research, Vol. 26, No. 11, 11.2016, p. 1176-1177.

Research output: Contribution to journal › Journal article › Commissioned

Harvard

Fiil, BK & Gyrd-Hansen, M 2016, 'OTULIN deficiency causes auto-inflammatory syndrome', Cell Research, vol. 26, no. 11, pp. 1176-1177. https://doi.org/10.1038/cr.2016.113

APA

Fiil, B. K., & Gyrd-Hansen, M. (2016). OTULIN deficiency causes auto-inflammatory syndrome. Cell Research, 26(11), 1176-1177. https://doi.org/10.1038/cr.2016.113

Vancouver

Fiil BK, Gyrd-Hansen M. OTULIN deficiency causes auto-inflammatory syndrome. Cell Research. 2016 Nov;26(11):1176-1177. https://doi.org/10.1038/cr.2016.113

Author

Fiil, Berthe Katrine ; Gyrd-Hansen, Mads. / OTULIN deficiency causes auto-inflammatory syndrome. In: Cell Research. 2016 ; Vol. 26, No. 11. pp. 1176-1177.

Bibtex

@article{6146b1bcde094732895c59824cf9ed6b,
title = "OTULIN deficiency causes auto-inflammatory syndrome",
abstract = "Ubiquitin chains assembled via the N-terminal methionine (Met1 or linear ubiquitin), conjugated by the linear ubiquitin chain assembly complex (LUBAC), participate in NF-κΒ-dependent inflammatory signaling and immune responses. A recent report in Cell finds that OTULIN, a deubiquitinase that selectively cleaves Met1-linked ubiquitin chains, is essential for restraining inflammation in vivo.",
keywords = "Endopeptidases, Immunity, Innate, Lymphocytes, Neurotransmitter Agents, Ubiquitin",
author = "Fiil, {Berthe Katrine} and Mads Gyrd-Hansen",
year = "2016",
month = nov,
doi = "10.1038/cr.2016.113",
language = "English",
volume = "26",
pages = "1176--1177",
journal = "Cell Research",
issn = "1001-0602",
publisher = "nature publishing group",
number = "11",

}

RIS

TY - JOUR

T1 - OTULIN deficiency causes auto-inflammatory syndrome

AU - Fiil, Berthe Katrine

AU - Gyrd-Hansen, Mads

PY - 2016/11

Y1 - 2016/11

N2 - Ubiquitin chains assembled via the N-terminal methionine (Met1 or linear ubiquitin), conjugated by the linear ubiquitin chain assembly complex (LUBAC), participate in NF-κΒ-dependent inflammatory signaling and immune responses. A recent report in Cell finds that OTULIN, a deubiquitinase that selectively cleaves Met1-linked ubiquitin chains, is essential for restraining inflammation in vivo.

AB - Ubiquitin chains assembled via the N-terminal methionine (Met1 or linear ubiquitin), conjugated by the linear ubiquitin chain assembly complex (LUBAC), participate in NF-κΒ-dependent inflammatory signaling and immune responses. A recent report in Cell finds that OTULIN, a deubiquitinase that selectively cleaves Met1-linked ubiquitin chains, is essential for restraining inflammation in vivo.

KW - Endopeptidases

KW - Immunity, Innate

KW - Lymphocytes

KW - Neurotransmitter Agents

KW - Ubiquitin

U2 - 10.1038/cr.2016.113

DO - 10.1038/cr.2016.113

M3 - Journal article

C2 - 27686184

VL - 26

SP - 1176

EP - 1177

JO - Cell Research

JF - Cell Research

SN - 1001-0602

IS - 11

ER -

ID: 280717847